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Query: UMLS:C0338671 (Steroids)
9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments in vitro on tissue from a feminizing adrenocortical carcinoma removed from a postmenopausal patient are described. Portions of the adrenal tumor were cultured. The effects of ACTH, prolactin, and other protein hormones on the synthesis and secretion of steroid hormones by the cultured tissue were studied. Steroids were extracted from the culture medium with ethyl acetate. Steroid production was determined by high resolution-mass fragmentography and by radioimmunoassay. Results suggest that in vitro neither growth hormone (GH) nor luteinizing hormone (LH), at the concentrations used, effectively stimulated the synthesis and secretion of estradiol-17beta by the adrenal tumor tissue. However, ACTH and prolactin with insulin, appearing to influence the action of both these hormones, stimulated the output of estradiol-17beta. Steroid was being synthesized during the 3-day culture period. The tumor tissue actively synthesized and secreted into the medium estrone as well as estradiol-17beta under the influence of ACTH and prolactin with insulin. Data also suggest that LH and GH were capable of influencing the synthesis and secretion of androstenedione by the tissue explants. No DNA sulphate was present in the media from the tumor tissue cultures before or after incubation with either ACTH or prolactin. Results from studies with normal adrenal tissue in culture indicated that DNA sulphate, DHA, and androstenedione were present in the culture medium after 3 days' incubation. In this report the concentration of endogenous estrone relative to estradiol-17beta and estradiol was found to be high. The effect of protein hormones, other than ACTH, on adenylate cyclase activity of this tumor tissue indicated a lack of specificity of the membrane receptor sites. High resolution-mass fragmentography had greater specificity than radioimmunoassay.
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PMID:In vitro synthesis of steroids by a feminising adrenocortical carcinoma: effect of prolactin and other protein hormones. 18 Jul 40

Mechanisms whereby glucocorticoids might inhibit growth are reviewed from the perspective of glucocorticoid effects on cell metabolism and growth. Although glucocorticoids given to patients decrease levels of growth hormone and possible somatomedins, the effect of glucocorticoids on growth is not reversed when growth hormone is given. Glucocorticoids inhibit cell growth in culture. Cell inhibition correlates with binding of steroids to the glucocorticoid receptors. Some tissues are very sensitive; others are insensitive. In cell culture, changes in sensitivity can be associated with changes in binding, but this is not always the case in tissues of the animal. The mechanisms of inhibition of cell growth are not known. It could be due to steroid-induced synthesis of inhibitory proteins or to blocking by receptor-steroid complexes of the synthesis of RNA. Steroids may affect uptake of substrates, e.g., glucose or amino acids, which in turn affects growth. The inhibitory actions of glucocorticoids on individual tissues may explain why these steroids inhibit growth in the animal. It is not known, however, how the steroid inhibits linear growth in mass or which cell types are most important targets for such effects.
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PMID:Mechanisms of glucocorticoid inhibition of growth. 36 26

Glucorticoid therapy inhibits statural growth. Alternate-day therapy causes less growth suppression than does daily therapy, and, in experimental animals and children with asthma, it has been associated with normal growth. Although catch-up growth may occur after cessation of steroid therapy, this is not always the case, especially when therapy has been prolonged. In children treated with steroids for glomerulonephritis or nephrotic syndrome and especially in children after renal transplantation, factors other than steroid therapy may contribute to growth retardation. Steroids may suppress growth by direct action on cell metabolism, by inhibition of growth hormone or somatomedin and/or by effects on calcium and phosphorus metabolism. Present knowledge of mechanisms of action and dose-response relationships is complete, and it is difficult to prescribe therapy which will achieve a predictable therapeutic effect without inhibiting growth.
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PMID:Growth and glucocorticoids in children with kidney disease. 36 32

The multihormonal regulation of the estrogen receptor in the liver of female rats was studied under in vivo conditions. The steroid receptor level was assayed by hormone binding and specific mRNA analyzed by solution hybridization using a 35S-labeled RNA probe complementary to the ligand-binding domain of the estrogen receptor gene. Serum growth hormone levels were measured and correlated to the effects of glucocorticoid and thyroid hormone administration on the estrogen receptor expression. In animals subjected to adrenalectomy plus thyroidectomy, the estrogen receptor concentration was reduced from 59 fmol/mg cytosol protein to 10 fmol/mg protein (i.e., with 87% relative to control animals). Adrenalectomy or thyroidectomy alone caused a decrease with 14% and 66%, respectively. Substitution with 10 micrograms betamethasone and 1 microgram triiodothyronine daily for 9 days completely restored the receptor content to control levels. Substitution with either hormone alone increased, but only partially restored receptor levels. The effect of betamethasone alone was dose dependent from 10 micrograms/d to 100 micrograms/d. This dose dependence was not seen when the animal simultaneously received 1 microgram of triiodothyronine. Superphysiologic doses of triiodothyronine did not raise estrogen receptor levels above those seen in animals treated with physiologic doses. High doses of triiodothyronine (greater than 20 micrograms/d) decreased serum growth hormone levels. The estrogen receptor mRNA levels in livers from hypophysectomized animals were increased after treatment with growth hormone (2.5-fold), thyroid hormone (two-fold), and glucocorticoids (1.5-fold). The results obtained indicate a very complex regulation of liver estrogen receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1991 Jul
PMID:Regulatory effects of growth hormone, glucocorticoids, and thyroid hormone on the estrogen receptor level in the rat liver. 178 Sep 53

Portacaval anastomosis causes delayed growth, decreased testes and liver weights, and elevated estradiol serum levels in male rats compared with sham-operated controls. Female rats treated with portacaval anastomosis grow at a normal rate despite changes in liver weight and estradiol levels similar to those observed in the male rats. This study examined the pituitary gonadal axis in both genders in this animal model. The rats receiving portacaval anastomosis were compared with both pair-fed and sham-operated control groups. Portacaval anastomosis decreased serum testosterone and increased estradiol in the male animals, while both testosterone and estradiol were increased in the females compared with gender-matched pair-fed and sham controls. Because pair feeding lowers male testosterone to a lesser extent, impaired nutrition may partially account for the decrease in the males treated with portacaval anastomosis. The ratio of estradiol to testosterone increased following anastomosis in male rats, but it was decreased in similarly treated females. Portacaval and anastomosis decreased luteinizing hormone without changing follicle-stimulating hormone in both male and female rats compared with sham-operated controls. Growth hormone was significantly decreased in male portacaval-treated rats compared with sham- and pair-fed animals. Increased insulin levels were found in both male and female pair-fed and portacaval anastomosis-treated animals. These data suggest that following portacaval anastomosis in rats, growth, serum testosterone, estradiol to testosterone ratios, and growth hormone are altered in a gender-specific manner with gender-independent changes in insulin and luteinizing hormone levels. These gender-specific effects may protect the portacaval anastomosis-treated female rat from growth retardation.
Steroids 1991 May
PMID:The influence of portacaval anastomosis on gonadal and anterior pituitary hormones in a rat model standardized for gender, food intake, and time after surgery. 187 62

The effect of insulin and insulin-like growth factor-1 (IGF-1) on progesterone secretion by porcine granulosa cells and their modulatory effect on follicle-stimulating hormone (FSH)-induced responses were examined. For comparative purposes, growth hormone (GH), previously shown to stimulate IGF-1 secretion, was also included. Granulosa cells from ovarian follicles (3 to 5 mm) were cultured in multiwell plates for the first 48 hours, either in the presence or absence of 1% fetal bovine serum (FBS). Following plating, all cultures were maintained in serum-free media. The addition of only insulin, but not IGF-1 or GH, enhanced progesterone secretion under both culture conditions. When low-density lipoprotein was provided as steroid substrate, a stimulatory effect of insulin on progesterone accumulation was observed with a minimum dose of 10 ng/ml. Granulosa cells cultured in serum-free media from the time of plating secreted less progesterone and were less responsive to FSH compared with cultures plated with 1% FBS. Only insulin, but not IGF-1, enhanced FSH responses to threefold in cells cultured with 1% FBS. However, when cells were cultured in serum-free media from the time of plating, both insulin and IGF-1, but not GH, potentiated the responses to FSH, but insulin was more potent than IGF-1. Insulin-like growth-factor-1 binding studies with granulosa cells indicate the presence of specific high-affinity binding sites (Kd 3.96 nM). A dose of 100 ng/ml of insulin had negligible cross-reactivity with IGF-1 receptors.
Steroids 1990 Mar
PMID:Comparative effects of insulin and insulin-like growth factor-1 on follicle-stimulating hormone-induced responses in porcine granulosa cells. 215 94

The effects of growth hormone (GH) +/- pregnant mare's serum gonadotropin (PMSG) on levels of insulin-like growth factor (IGF)-I and -II and IGF binding protein (BP)-2 and -3 in serum and follicular fluid (FFI) and on the expression of their mRNA in the ovaries of prepubertal gilts were determined. Steroids in FFI were also quantified. In the first experiment, GH, given for either 20 or 40 days, caused a distinct (threefold, p < 0.05) increase in IGF-I in both serum and FFI with no change in the FFI:serum ratio (0.65). Effects of GH on IGF-II were opposite, with a drop in circulating and FFI levels (p < 0.05). In contrast to data for IGF-I, FFI levels were higher than those in serum for IGF-II (1.42, FFI:serum); IGF-II levels and the ratio fell after GH treatment. GH for either 20 days or 40 days increased serum IGBP-3 to 140% and 250% of control values while decreasing serum IGFBP-2 by 46% and 31%, respectively (p < 0.001). FFI IGFBP-3 was increased to a similar extent by GH (p < 0.005), but IGFBP-2 was not affected. Neither progesterone (P4) nor estradiol (E2) was affected by treatment with GH. However, androstenedione (A4) was decreased by 20-day and 40-day GH treatment relative to the respective controls (p < 0.05). In the second experiment, PMSG resulted in a modest (28%) increase in intrafollicular IGF-I (p < 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of growth hormone and gonadotropin on the insulin-like growth factor system in the porcine ovary. 750 57

The use of the synthetic progestin medroxyprogesterone acetate (MPA) for estrus prevention in the dog can result in overproduction of growth hormone, suppression of plasma glucocorticoid levels, and the induction of mammary tumors. Proligestone (PROL) was claimed to be devoid of these unwanted side effects. In the present study, the binding characteristics of MPA and PROL for the canine progesterone receptor (PR) and glucocorticoid receptor (GR) were investigated. The apparent inhibition constants for the PR and GR of MPA and PROL were compared with those of progesterone, ORG 2058, and a number of corticosteroids. MPA and PROL had high affinities for both the PR and the GR. The rank order for displacement of the binding of the PR ligand [3H]ORG 2058 from the canine uterine receptor was: MPA approximately ORG 2058 > PROL > progesterone >> cortisol, dexamethasone, and spironolactone. The rank order for displacement of the specific binding of the GR ligand [3H]dexamethasone from the canine liver receptor was: dexamethasone > cortisol > MPA > PROL > progesterone >> aldosterone approximately spironolactone. The apparent inhibition constants of PROL for both the PR and the GR were approximately 10 times higher than those of MPA. The ratios of the inhibition constants for the GR and PR appeared to be equal for PROL and MPA. It is concluded that although MPA has higher affinities for the PR and GR than PROL, both progestins have a similar in vitro binding specificity, which is less than that of progesterone. These findings are consistent with suppression of the adrenal cortex and the induction of growth hormone secretion in the mammary gland after MPA and PROL treatment in dogs.
Steroids 1996 Mar
PMID:Binding specificity of medroxyprogesterone acetate and proligestone for the progesterone and glucocorticoid receptor in the dog. 885 30

The purpose of this study was to assess the influence of male, female and fetal cord sera, follicular fluid, and seminal plasma on human sperm-zona pellucida binding, using the hemizona assay. Steroids, gonadotrophins, growth hormone and prolactin concentrations in follicular fluid and sera were also analysed. The influence of follicular fluid (10 or 50%, v/v) and sera (10%) on sperm-zona pellucida binding was investigated by supplementing the sperm processing medium as well as the sperm-hemizona incubation medium. Different seminal plasma concentrations (1 or 10%) were added to the sperm-hemizona incubation medium. Supplementation with 10% day 3 donor serum was used as a control throughout experimentation. Although supplementation with male sera and fetal cord serum exerted a stimulatory effect (36 and 90% respectively; P < 0.029) on sperm-zona pellucida binding, hemizona indices obtained with addition of male sera, fetal cord serum and sera obtained from sub-fertile in-vitro fertilization (IVF) patients on day 12 of their menstrual cycle did not differ significantly (P > 0.05). Final progesterone concentrations in sperm-zona pellucida incubation media (10% follicular fluid supplementation), which ranged from 0.788 to 3.85 microg/ml, enhanced sperm binding to the zonae by >100% (P < 0.02). The utilization of follicular fluid (10%) as a natural physiological stimulus to enhance sperm-zona pellucida binding in an IVF setting is recommended. The presence of seminal plasma in the spermzona pellucida incubation media showed no beneficial effect on the binding ability of sperm, and can be viewed as an unfavourable substance in the proximity of the oocyte.
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PMID:The influence of sera, follicular fluids and seminal plasma on human sperm-zona pellucida binding. 915 44

Estrogen treatment affects the hepatic synthesis and/or secretion of several proteins involved in clinically important pathological processes such as atherosclerosis, hypertension, and thrombosis. The endocrine regulation of the estrogen receptor (ER) concentration in primary cultures of rat hepatocytes was studied. Human growth hormone (hGH) and dexamethasone (DEX) in combination increased ER concentration 6-fold and ER mRNA levels 2.5-fold. These effects were not significantly different from those observed after treatment with the purely somatogenic bovine growth hormone (GH) in combination with DEX. Treatment with the lactogen ovine prolactin in the presence or absence of DEX did not significantly affect ER or ER mRNA concentrations. Triiodothyronine treatment at the most effective concentration (50 nM) increased ER and ER mRNA levels twofold. Medium supplementation with estradiol (0.1 nM) throughout the experiment did not affect the response to treatment with hGH and DEX. Treatment with high concentrations of ethinylestradiol in combination with hGH and DEX, however, increased the ER level twice as much as hGH and DEX without addition of estradiol or ethinylestradiol, whereas the ER mRNA concentration was the same in both the GH+DEX group and GH+ DEX+ (estradiol or ethinylestradiol) groups. These data indicate the importance of GH in combination with glucocorticoids for the maintenance of ER concentrations in the rat liver. Thyroid hormones may be of some, although minor importance, whereas the data suggest that prolactin is not directly involved in hepatic ER regulation.
Steroids 1997 Oct
PMID:Hormonal regulation of the estrogen receptor in primary cultures of hepatocytes from female rats. 938 11


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